Neuroprotection of geniposide against hydrogen peroxide induced PC12 cells injury: involvement of PI3 kinase signal pathway |
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基金项目: | Acknowledgements This work was supported by grants from the National Natural Science Foundation of China (30600813, 30701020), the Program for New Century of Excellent Talents in University (NCET-07-0913), and the Chongqing Science & Technology Commission (CSTC, 2007AA5029), and partly by grants from the Ministry of Science and Technology of China ("973 project", 2003CB716601) |
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摘 要: | Aim: Oxidative stress plays a critical role in the pathogenic cascade leading to neuronal degeneration in AD. Consequently, the induction of endogenous antioxidative proteins by antioxidants seems to be a very reasonable strategy for delaying the disease's progression. In previous work, we identified the neurotrophic and neuroprotective effects of geniposide, which result from the activation of glucagon-like peptide I receptor (GLP-1R). In this study, we explore the role of PI3 kinase signaling pathway in the neuroprotection of geniposide in PC12 cells. Methods: Cell viability was determined by MTT assay. Apoptosis was detected by Hoechst and PI double staining. The protein expression of Bcl-2 and phosphorylation of Akt308, Akt473, GSK-313, and PDK1 was measured by Western blot. Results: Geniposide induced the expression of the antiapoptotic protein Bcl-2, which inhibited apoptosis in PC12 cells induced by H202, and this effect could be inhibited by preincubation with LY294002, a selective inhibitor of PI3K. Further-more, geniposide enhanced the phosphorylation of Akt308, Akt473, GSK-313 and PDK1 under conditions of oxidative stress. Conclusion: These results demonstrate that the PI3K signaling pathway is involved in the neuroprotection of geniposide in PC12 cells against the oxidative damage induced by H202 in PC12 cells.
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关 键 词: | 胰高血糖素 受体 PI3K GSK-3β PDK1 蛋白质 |
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